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Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

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Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
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Depolarizing Blockers: Mechanism of Action01:28

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
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Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

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Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
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Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

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Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
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Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
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Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

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Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
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Related Experiment Video

Updated: Aug 6, 2025

Dual-Dye Optical Mapping of Hearts from RyR2R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia
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Remdesivir-induced conduction abnormalities: A molecular model-based explanation.

Ryan Kingsley1, Christopher Rohlman2, Ashley Otto3

  • 1Division of Hospital Medicine, Mayo Clinic, Rochester, MN, United States.

Journal of Pharmacy & Pharmaceutical Sciences : a Publication of the Canadian Society for Pharmaceutical Sciences, Societe Canadienne Des Sciences Pharmaceutiques
|March 21, 2023
PubMed
Summary
This summary is machine-generated.

Remdesivir may cause cardiac issues in COVID-19 patients. Molecular modeling suggests its metabolite, GS-441524, could activate cardiac adenosine A1 receptors, explaining these side effects.

Keywords:
COVID-19GS-441524adenosinecardiac conduction abnormalitiesconduction abnormalitiesremdesivir

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Area of Science:

  • Pharmacology
  • Molecular Biology
  • Cardiology

Background:

  • Remdesivir is an antiviral medication used for COVID-19.
  • Cardiac conduction abnormalities have been observed in patients treated with remdesivir.
  • The underlying mechanism for these cardiac side effects remains unclear.

Purpose of the Study:

  • To investigate the proposed mechanism linking remdesivir metabolite GS-441524 to cardiac adenosine A1 receptor activation.
  • To assess the feasibility of GS-441524 causing cardiac conduction abnormalities through molecular modeling.

Main Methods:

  • Acquired molecular structures of adenosine and GS-441524 from PubChem.
  • Utilized UCSF Chimera for ligand docking simulations.
  • Selected models based on binding affinity and root mean square deviation.

Main Results:

  • Molecular modeling demonstrated feasible docking compatibility between GS-441524 and the adenosine A1 receptor.
  • The study supports the hypothesis that GS-441524 can activate cardiac adenosine A1 receptors.

Conclusions:

  • The proposed mechanism of exogenous cardiac A1 receptor activation by GS-441524 is viable.
  • This mechanism may explain cardiac conduction abnormalities associated with remdesivir use in COVID-19.
  • Further research is required to establish causality.